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Topics in Geriatric Rehabilitation • Volume 34, Number 4, 262-268 • Copyright © 2018 Wolters Kluwer Health, Inc. All rights reserved.
DOI: 10.1097/TGR.0000000000000203
Background: One of the most disabling problems in 
Parkinson disease (PD) is gait impairment. Noninvasive brain 
stimulation techniques, such as transcranial direct current 
stimulation (tDCS), have been introduced as a therapeutic 
alternative for coping with PD motor problems. However, the 
effects of tDCS on gait performance in PD have not yet been 
fully established. Therefore, the main objective of this study 
was to evaluate whether a single session of tDCS modifies 
gait kinematics in individuals with PD.
Methods: Twenty-one individuals with PD were included in 
this randomized, double-blinded, sham-controlled design 
study. They were randomly allocated in one real (N = 8) or 
sham (N = 9) tDCS group. Real tDCS comprises a 2-mA 
anodic current applied over 15 minutes in the supplemen-
tary motor area and medial areas of the primary motor 
cortices through a bipolar electrode montage. Gait kinemat-
ics and the Unified Parkinson’s Disease Rating Scale Part III 
(UPDRS-III) were assessed before and immediately after a 
single stimulation session. Pre- minus poststimulation (Δ) 
values were computed and compared through a Mann-
Whitney test. Data are shown as the median (lower, upper 
quartile).
Results: There was a significant group difference with a 
large effect size for Δ values of gait cadence (P = .014, d = 
0.87), indicating its reduction after anodic stimulation in the 
real (−0.28 [−1.16, 0.01] steps/s) compared with sham 
tDCS group (0.17 [0.00, 0.40] steps/s). No other significant 
effect was found.
Conclusion: The findings of this study suggest that anodic 
tDCS administered in a single session improves gait cadence 
in PD individuals.
Key words: mobility, neuromodulation, Parkinson disease, 
physiotherapy, rehabilitation, transcranial direct current 
stimulation
Effects of Acute Transcranial Direct Current 
Stimulation on Gait Kinematics of Individuals 
With Parkinson Disease
Débora Cristina Lima da Silva, MSc; Thiago Lemos, DSc; Arthur de Sá Ferreira, DSc; 
Carlos Henrique Ramos Horsczaruk, MSc; Carla Andressa Pedron, PT; Erika de Carvalho Rodrigues, DSc; 
Laura Alice Santos de Oliveira, DSc
Gait impairment is one of the main and more debili-tating symptoms faced by individuals with Parkin-son disease (PD), and it is associated with func-
tional deficits, episodes of falls, increased morbidity, and 
reduced life expectancy.1-3 Gait in PD is hypokinetic, with 
reduced stride length, increased gait cadence, decreased 
gait velocity, reduced arm swinging, and predominance of 
a flexor posture.4-6 Current available pharmacological or 
surgical interventions such as deep brain stimulation have 
limited effects on gait impairments commonly found in 
PD.7 Some of these effects can even have detrimental 
effects over gait parameters.8 Therefore, new approaches 
to gait deficit management in PD need to be explored.
Noninvasive brain stimulation is among the most prom-
ising alternatives for motor rehabilitation in PD.9-16 Particu-
larly, transcranial direct current stimulation (tDCS) is an 
easy-to-use, safe, portable, and low-cost technique, show-
ing high tolerability and long-lasting effects.17 The use of 
tDCS on PD rehabilitation combined with physical ther-
apy or other types of brain stimulation has been recently 
explored, but its effects on motor symptoms remain 
inconclusive.11-13,16
Particularly, there is sparse evidence of the effect of 
noninvasive brain stimulation with regard to gait impair-
ments in PD patients. Elsner et al18 performed a systematic 
review on the topic and found no evidence of improve-
ment in tDCS-based therapy on gait speed assessed using 
timed gait measurements (eg, Timed Up & Go [TUG] test 
and a 10-m walk test). However, applying a combined 
approach to stimulate the primary motor cortex (using 
Author Affiliations: Programa de Pós-Graduação em Ciências da Reabili-
tação, Centro Universitário Augusto Motta (UNISUAM), Rio de Janeiro, 
Brazil (Mss Silva, Pedron, Rodrigues, and Oliveira and Messrs Lemos, 
Ferreira, and Horsczaruk); Instituto D’or de Pesquisa e Ensino, IDOR, Rio 
de Janeiro, Brazil (Ms Rodrigues); and Instituto Federal de Educação, 
Ciência e Tecnologia do Rio de Janeiro, IFRJ, Rio de Janeiro, Brazil (Ms 
Oliveira).
The authors have disclosed that they have no significant relationships 
with, or financial interest in, any commercial companies pertaining to this 
article.
Clinical Trial Register: RBR-4hvfzj (www.ensaiosclinicos.gov.br/rg/RBR-
4hvfzj).
Correspondence: Laura Alice Santos de Oliveira, DSc, Programa de Pós 
Graduação em Ciências da Reabilitação, Centro Universitário Augusto da 
Mota (UNISUAM), Praça das Nações, 34, 3 andar, CEP: 21041-020, Rio 
de Janeiro, RJ, Brazil (laura.oliveira@ifrj.edu.br).
http://www.ensaiosclinicos.gov.br/rg/RBR-4hvfzj
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Topics in Geriatric Rehabilitation www.topicsingeriatricrehabilitation.com 263
1-Hz repetitive transcranial magnetic stimulation precondi-
tioned by anodal tDCS), von Papen et al19 found improve-
ments in gait performance by measuring gait kinematics. 
Since hypoactivation of the supplementary motor area 
(SMA) is related to PD motor symptoms in general, particu-
larly gait disturbances,20,21 we aimed to stimulate this spe-
cific medial motor area together with the medial part of the 
primary motor cortices (M1) with tDCS where the lower-
limb muscle representation is located. The effect of a single 
application of tDCS on gait features, such as stride length, 
gait cadence, velocity, and ankle joint angles, together with 
the motor signs of individuals with PD, was investigated. 
We hypothesized that the bilateral stimulation of SMA and 
M1 would have beneficial effects on the gait kinematics 
of individuals with PD. Understanding the acute effect of 
tDCS on gait performance might provide important infor-
mation on the development of new stimulation protocols 
to allow for a better design of the intervention for this dis-
ability in PD individuals.
MATERIAL AND METHODS
Participants and design
This was a randomized, double-blinded, sham-controlled 
study design. Inclusion criteria were the following: diagno-
sis of idiopathic PD by a neurologist; a Hoehn & Yahr stage 
of 2 to 3; aged 50-80 years; ability to walk 10 m without assis-
tive devices; and regular medication usage for PD. Individu-
als with Mini-Mental Examination score 18 or less, other 
neurological diseases, suspected or confirmed pregnancy, 
metallic implants, pacemakers, a history of epilepsy, other 
disorders affecting gait and balance, uncorrected visual 
impairment, and dizziness were not included. Individuals 
from a local rehabilitation center were invited to participate 
(Figure 1). After an interview that was part of the eligibility 
criteria search, 21 individuals were selected and accepted 
the invitation. The institutional ethics committee approved 
this study prior to its execution (CAAE 29496514.2.0000. 
5235). The study was registered in the Brazilian Clinical 
Trials Registry (ReBec) with the number RBR-4hvfzj (www.
ensaiosclinicos.gov.br/rg/RBR-4hvfzj). Every participant pro-
vided written informed consent prior to the experiment.
Procedures
All participants were previously enrolled in a group-
based exercise program (10 sessions, 1 hour, 3 times a 
week), designed to cope with motor symptoms in PD. 
Participants underwent a session of clinical and behavio-
ral assessments (preintervention) that included the Uni-
fied Parkinson’s Disease Rating Scale Part III (UPDRS-III) 
and a gait kinematic analysis. Previously, a researcher not 
involved in thestudy performed a randomization (www.
randomization.com) to allocate the 21 participants in 
one of the following 2 groups: the REAL group, which 
received anodal tDCS (n = 11), and the SHAM group, 
which received fictitious stimulation and represented 
Figure 1. Diagram representing the flow of participants at each stage of the study. tDCS indicates transcranial direct 
current stimulation.
http://www.ensaiosclinicos.gov.br/rg/RBR-4hvfzj
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264 www.topicsingeriatricrehabilitation.com October–December 2018
the control group (n = 10). One researcher programed 
and performed the stimulation session for each patient. 
After the stimulation session, all participants underwent 
the same clinical and behavioral assessments (postinter-
vention). Both the volunteers and the examiners 
remained blinded to the type of stimulation that each 
group received. All procedures were performed during 
the “on” period of medication (approximately 1 hour 
after drug intake).
Transcranial direct current stimulation
A stimulator (NeuroConn equipment–DC, Ilmenau, 
Germany) delivered a continuous direct current by a saline-
soaked pair of surface sponge electrodes (35 cm2). The 
anode was positioned 1.8 cm anterior to the vertex, corre-
sponding approximately to the location of M1 and SMA.22 
The cathode was positioned over the supraorbital area ipsi-
lateral to the most affected side. Participants of the tDCS 
group received electrical stimulation of 2 mA during 
15 minutes. The current intensity was ramped up over 
10 seconds and decreased similarly. The participants in the 
sham group received the same stimulation, only over 
30 seconds. At the end of the stimulation session, the 
examiner monitored the occurrence of adverse effects 
using a specific questionnaire applied to both groups.23
Gait kinematics analysis
Kinematics gait parameters were obtained from all par-
ticipants using an optoelectronic system (Qualisys MEDI-
CAL AB, Gothenburg, Sweden). Reflective markers were 
fixed in both lower limbs of the participants on some 
anatomical structures. Only the calcaneal, lateral malleo-
lus, and metatarsophalangeal joints of the fifth finger 
were used in the analysis. For data acquisition, 4 infrared 
cameras (ProReflex MCU 240, Gothenburg, Sweden) 
were used to capture the passive markers affixed to the 
patient’s body. The system was calibrated according to 
the manufacturer’s instructions before data acquisition. 
Participants were required to walk in their usual velocity 
along a 10-m corridor, to turn around, and to return to 
the starting point. Data captured in the ranges of 0 to 2 
m and 8 to 10 m were discarded from analysis to exclude 
transients related to gait initiation, turning around, and 
gait termination. The analyzed data thus comprised a 
6-m walkway at the middle of the corridor. Sampling fre-
quency was set to 200 Hz.
Movements were analyzed according to mediolateral 
(X), longitudinal (Y), and vertical (Z) axes. The recon-
struction of the location of reflective markers was per-
formed using Qualisys Track Motion 2.4 (Qualisys MEDI-
CAL AB). The gait data of each patient were exported to 
the R software 3.1 (R Core Team, Foundation for Statistical 
Computing, Vienna, Austria,) for further processing and 
analysis. Markers’ positions were low-pass filtered using a 
centered moving average procedure (35 samples, cutoff 
∼15 Hz) before calculation of linear velocity and accel-
eration using the derivative method. Gait cycles were 
identified using single thresholds for linear displacement 
of the calcaneus as a reference marker for the respective 
body side. Data from 3 individuals of the REAL and 3 of 
the SHAM group were lost because of technical problems 
during acquisition for the right leg. Thus, only the data 
relative to 8 individuals in the tDCS group and 9 in the 
sham group were analyzed.
The spatiotemporal variables calculated were as follows: 
stride length (meters; sum of the length of all strides in the 
visible route area per the number of strides); gait cadence 
(strides/min; number of gait cycles on the visible route 
divided by the duration of all strides on the visible route); 
gait duration (seconds; sum of the duration of all strides 
in the visible per stride route); and gait speed (m/s; aver-
age of the ratio between the length of each stride and its 
respective duration). The angular variable was estimated 
from ankle joint motion (dorsiflexion and plantar flexion). 
The mean value of all cycles was used as the representative 
value whenever a patient exhibited more than 1 complete 
gait cycle.
Unified Parkinson’s Disease Rating Scale Part III
The UPDRS is a classical scale for the assessment of disabil-
ity and impairment in individuals with PD.24 The UPDRS 
evaluates the signs and symptoms of PD and activity level, 
both self-reported and through clinical observation by the 
examiner. The scale has 4 parts and is used to monitor dis-
ease progression and treatment efficacy. The guidelines of 
the Movement Disorders Society for evaluation of PD 
motor tasks are described in part III of the UPDRS docu-
ment (UPDRS-III), which comprises 14 items. For each 
item, scores range from 0 (“best”) to 4 (“poorest motor 
performance”) in each task.24
Statistical analysis
Pre- minus poststimulation (ΔtDCS) values were com-
puted for each gait-derived variable. On the basis of the 
non-Gaussian distribution of these variables (Shapiro-
Wilks’s P < .02), a Mann-Whitney test for independent 
measures was applied for real versus sham tDCS group 
comparison, with the α level set at 5%. A nonparametric 
Cohen’s d value was estimated25 and was considered as 
trivial (d < 0.10), small (0.10 < d < 0.30), medium (0.30 < 
d < 0.50), or large (d > 0.50). Demographic and clinical 
characteristics were compared between groups with an 
independent t test (mean ± SD) or χ2 test (number of 
occurrences). All analyses were performed using SPSS soft-
ware (IBM, Armonk, New York).
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Topics in Geriatric Rehabilitation www.topicsingeriatricrehabilitation.com 265
RESULTS
No significant between-group statistical differences were 
found regarding the demographic and clinical characteris-
tics of the sample (Table 1).
No participant reported adverse events associated with 
the stimulation session. The descriptive data of the out-
come measures before and after the stimulations are pres-
ent in Table 2.
There was a significant difference between groups for 
gait cadence (z = −2.454, P = .014) as well as a large 
effect size (d = 0.87; see Table 2). For all other variables, 
there were no significant differences between groups 
(all Ps > .178; Table 2). Nevertheless, a medium effect 
size was observed for stride length (d = 0.37), gait dura-
tion (d = 0.34), and ankle dorsiflexion angle (d = 0.48; 
see Table 2). Figure 2 displays a plot detailing pre- and 
post-tDCS.
DISCUSSION
The main finding of the present study was a decrease in 
gait cadence and trends of an increase in stride length and 
gait duration for the tDCS compared with the sham group. 
This finding may indicate that after a single tDCS session of 
stimulation of SMA and medial areas of M1, the individuals 
spent more time to cross the same area with larger strides. 
TABLE 2 Values Referring to the Variables Assessed During Gait Task From PD Individuals of 
Real and Sham tDCS Groupsa
Real tDCS (n = 8) Sham tDCS (n = 9) M-W Test
Pre Post Δ Pre Post Δ P d
UPDRS-III 35.5
(27.5, 37.0)
28.0
(20.5, 32.5)
−6.0
(−8.0, −3.5)
29.0
(24.0, 37.0)
25.0)
(21.0, 31.0)
−4.00
(−11.0, −3.0)
.923 0.03
Stride length, m 0.97
(0.89, 1.03)
1.04
(0.99, 1.17)
0.08
(−0.03, 0.15)
1.14
(0.98, 1.20)
1.11
(0.95, 1.27)
−0.03
(−0.05, 0.09)
.290 0.37
Cadence, n/s 0.98
(0.79, 1.83)
0.66
(0.61, 0.83)
−0.28
(−1.16, 0.01)
0.80
(0.78, 0.91)
0.95(0.81, 0.97)
0.17
(0.00, 0.40)
.014 0.87
Gait duration, s 1.05
(1.00, 1.22)
1.10
(1.02, 1.35)
0.01
(−0.05, 0.15)
1.21
(1.10, 1.25)
1.06
(1.04, 1.24)
−0.03
(−0.22, 0.06)
.336 0.34
Gait speed, m/s 0.88
(0.74, 1.02)
0.87
(0.77, 0.97)
0.05
(−0.01, 0.12)
0.90
(0.83, 0.94)
0.89
(0.68, 1.04)
0.04
(−0.13, 0.06)
.560 0.22
Dorsiflexion (R) 7.98
(2.96, 10.32)
7.00
(5.74, 13.58)
3.29
(−0.68, 4.62)
10.76
(7.29, 13.29)
10.73
(5.96, 12.66)
−0.63
(−5.29, 2.95)
.178 0.48
Plantar flexion (R) −10.23
(−24.09, 
−1.02)
−15.77
(−22.46, 
−7.93)
−1.46
(−17.72, 
7.76)
−3.13
(−13.75, 
−0.99)
−6.04
(−10.26, 
−1.01)
1.12
(−9.70, 8.98)
1.000 0.00
Abbreviations: d, Cohen’s effect size; M-W, Mann-Whitney test for real tDCS versus sham tDCS comparison of Δ value; PD, Parkinson disease; R, right limb; tDCS, 
transcranial direct current stimulation; UPDRS-III, Unified Parkinson’s Disease Rating Scale Part III.
aData are present as median (lower, upper quartile). Dorsiflexion and plantar flexion angles are expressed in degrees.
TABLE 1 Demographic and Clinical Variables 
for Each Groupa
Real tDCS 
(n = 8)
Sham tDCS 
(n = 9) P b
Age, y 66 ± 5 66 ± 10 .968
Disease duration, y 6 ± 6 5 ± 1 .674
MMSE (score) 27 ± 2 25 ± 2 .122
Gender
 Male, n 4 6 .317
 Female, n 4 3
HY stage
 Stage 2, n 4 2 .117
 Stage 2.5, n 3 7
 Stage 3, n 1 0
Abbreviations: HY, Hoehn & Yard Modifying Staging scale; MMSE, Mini-Mental 
State Examination; tDCS, transcranial direct current stimulation.
aData are presented as the mean ± SD or number of occurrences (n).
bP value from a t test for independent measures (age, disease duration, and 
MMSE) or χ2 test (gender and HY stage).
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266 www.topicsingeriatricrehabilitation.com October–December 2018
For the UPDRS-III scores, there were no statistical differ-
ences between groups, suggesting a lack of effect of the 
stimulation session over the general motor aspects of PD.
It was already described that, among other changes, 
the gait in PD is hypokinetic, with reduced stride length, 
decreased gait velocity, shorter stepping, reduced arm 
swinging, and predominance of flexor posture when 
compared with age-matched control individuals.6 
Individuals with PD have a reduced stride length, which 
they attempt to compensate for by heavily increasing the 
gait cadence.4,5 In fact, many studies described an increased 
gait cadence in individuals with PD.4,26 Other studies defend 
that the decreasing stride length in individuals with PD can 
be a compensatory strategy to maintain stability by limiting 
the displacement of the center of mass relative to the base 
of support.27,28 Irrespective of the underlying mechanism, 
these alterations have a huge impact over mobility and 
quality of life in individuals with PD.26,29 In the present study, 
a single session of anodal tDCS seems to partially improve 
this impaired gait pattern by decreasing gait cadence. Angu-
lar data did not change after the stimulation session, at least 
at the ankle level, suggesting that such an effect on gait 
cadence cannot be attributed to the ankle kinematics after 
the stimulation. Nevertheless, we cannot rule out that the 
changes of gait cadence may result from an increment of 
the excursion of the hip or knee joints because these data 
were not captured; thus, further investigation is required.
Few studies have focused on evaluating the effects of 
a single tDCS session on gait. Those that have, however, 
used timed gait measures (eg, TUG and a 10-m walk test) 
that do not allow a kinematic analysis of gait and/or found 
conflicting results. Benninger et al11 applied anodal tDCS 
over M1 and dorsolateral prefrontal cortex in 8 sessions 
of alternating day pacing and evaluated bradykinesia 
(UPDRS) and gait velocity (10-m walk test—TC10m) dur-
ing the “on” and “off ” phases of the medication. When 
comparing the results between groups, a decrease in 
TC10M duration for the REAL group was observed only 
at the “off ” period of the medication but not for the “on” 
period. When the gait velocity at baseline was compared 
with the performance after 24 hours of stimulation, an 
increase in velocity was found for both groups in both 
phases of the pacing independent medication. In the 
present study, the effects of real and sham stimulation 
were tested using the same stimulation site, with statisti-
cal improvements and a large effect size on gait cadence 
immediately after the stimulation.
Both Kaski et al13 and Costa-Ribeiro et al16 applied 
anodal tDCS over cerebral sites some centimeters prior 
to Cz and associated physical training during the “on” 
period. Kaski et al13 applied tDCS during balance and gait 
training, whereas Costa-Ribeiro et al16 trained gait by using 
visual cues after the tDCS session. Only Kaski et al13 found 
improvements in gait velocity and an increment of stride 
length after the treatment period. In the present study, 
the aim was to evaluate the isolated effect of tDCS on gait 
kinematics. A statistical decrease in gait cadence with a 
large effect size was found for the individuals in the REAL 
group compared with the SHAM group. These results refer 
only to the right leg. However, it is important to consider 
that the sample in the Hoehn & Yard participants’ score 
denoted bilateral impairment.
Figure 2. Representative data (participant 15) of gait kinematic analysis showing the right (right-sided panels) and left (left-
sided panels) calcaneus vertical height before (upper panels) and after transcranial direct current stimulation (lower panels).
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Topics in Geriatric Rehabilitation www.topicsingeriatricrehabilitation.com 267
Regarding UPDRS-III scores, there are some contro-
versial findings after tDCS. Some studies that employed 
a single session or fewer than 5 sessions of anodal tDCS 
over M1 found an improvement in UPDRS-III scores,14,10 
whereas other studies11,30 did not (although Benninger 
et al11 found an improvement in this measure when they 
employed composite UPDRS scores that took into consid-
eration only the features related to bradykinesia). A recent 
Cochrane systematic review18 found no evidence of effect 
regarding UPDRS scores in the 2 studies included.11,14 The 
UPDRS may not be an ideal outcome measure to evaluate 
the effects of the anodal stimulation since the motor sec-
tion of this instrument takes into account not only differ-
ent parts of the body but also different cardinal symptoms 
of PD. More studies are still necessary to confirm the effect 
of anodal tDCS over UPDRS scores in individuals with PD.
The present study presents some limitations. We exam-
ined a small sample size of individuals with only mild PD 
stages while “on” medication. These features can limit 
the external validity of the stimulation effect. Nonethe-
less, the observed large effect sizes on gait cadence and 
medium effect sizes for other gait parameters increase 
our confidence in data interpretation. Further studies 
employing the suggested tDCS protocol combined with 
balance training, in addition to testing additional training 
sessions, are needed to evaluate the therapeutic use of 
the protocol in patients with PD.
CONCLUSIONS
Our findings indicate a difference between groups for the 
gait cadence variable when comparing the REAL and SHAM 
groups. The next step is to determine whether the same 
stimulation employed here would bring some additional 
benefits for gait kinematics in PD when applied in associa-
tion with physical exercises.
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